scholarly journals Galectins as Emerging Glyco-Checkpoints and Therapeutic Targets in Glioblastoma

2021 ◽  
Vol 23 (1) ◽  
pp. 316
Author(s):  
Guillermo A. Videla-Richardson ◽  
Olivia Morris-Hanon ◽  
Nicolás I. Torres ◽  
Myrian I. Esquivel ◽  
Mariana B. Vera ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Transformation ◽  
Adult Population ◽  
Antiangiogenic Therapy ◽  
Therapeutic Targets ◽  
Treatment Modalities ◽  
Migration And Invasion ◽  
Oncogenic Signaling ◽  
Tumor Cell Migration ◽  
Cell Death Pathways

Despite recent advances in diagnosis and treatment, glioblastoma (GBM) represents the most common and aggressive brain tumor in the adult population, urging identification of new rational therapeutic targets. Galectins, a family of glycan-binding proteins, are highly expressed in the tumor microenvironment (TME) and delineate prognosis and clinical outcome in patients with GBM. These endogenous lectins play key roles in different hallmarks of cancer by modulating tumor cell proliferation, oncogenic signaling, migration, vascularization and immunity. Additionally, they have emerged as mediators of resistance to different anticancer treatments, including chemotherapy, radiotherapy, immunotherapy, and antiangiogenic therapy. Particularly in GBM, galectins control tumor cell transformation and proliferation, reprogram tumor cell migration and invasion, promote vascularization, modulate cell death pathways, and shape the tumor-immune landscape by targeting myeloid, natural killer (NK), and CD8+ T cell compartments. Here, we discuss the role of galectins, particularly galectin-1, -3, -8, and -9, as emerging glyco-checkpoints that control different mechanisms associated with GBM progression, and discuss possible therapeutic opportunities based on inhibition of galectin-driven circuits, either alone or in combination with other treatment modalities.

Phosphorylated Caveolin-1 Regulates Rho/ROCK-Dependent Focal Adhesion Dynamics and Tumor Cell Migration and Invasion

2008 ◽  
Vol 68 (20) ◽  
pp. 8210-8220 ◽  
Author(s):  
Bharat Joshi ◽  
Scott S. Strugnell ◽  
Jacky G. Goetz ◽  
Liliana D. Kojic ◽  
Michael E. Cox ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Focal Adhesion ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tumor Cell Migration ◽  
Caveolin 1

scholarly journals Metastasis-associated protein 1 drives tumor cell migration and invasion through transcriptional repression of RING finger protein 144A.: FIGURE 3.

2012 ◽  
Vol 287 (15) ◽  
pp. 12158-12158
Author(s):  
Hezlin Marzook ◽  
Da-Qiang Li ◽  
Vasudha S. Nair ◽  
Prakriti Mudvari ◽  
Sirigiri Divijendra Natha Reddy ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Transcriptional Repression ◽  
Ring Finger ◽  
Migration And Invasion ◽  
Ring Finger Protein ◽  
Cell Migration And Invasion ◽  
Tumor Cell Migration ◽  
Finger Protein

scholarly journals The RabGEF ALS2 is a hypoxia inducible target associated with the acquisition of aggressive traits in tumor cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Solange Rivas ◽  
Patricio Silva ◽  
Montserrat Reyes ◽  
Hugo Sepúlveda ◽  
Luis Solano ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Tumor Cell ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Proximal Promoter ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tumor Cell Migration ◽  
Rab Protein

AbstractTumor hypoxia and the hypoxia inducible factor-1, HIF-1, play critical roles in cancer progression and metastasis. We previously showed that hypoxia activates the endosomal GTPase Rab5, leading to tumor cell migration and invasion, and that these events do not involve changes in Rab protein expression, suggesting the participation of intermediate activators. Here, we identified ALS2, a guanine nucleotide exchange factor that is upregulated in cancer, as responsible for increased Rab5-GTP loading, cell migration and metastasis in hypoxia. Specifically, hypoxia augmented ALS2 mRNA and protein levels, and these events involved HIF-1α-dependent transcription, as shown by RNAi, pharmacological inhibition, chromatin immunoprecipitation and bioinformatics analyses, which identified a functional HIF-1α-binding site in the proximal promoter region of ALS2. Moreover, ALS2 and Rab5 activity were elevated both in a model of endogenous HIF-1α stabilization (renal cell carcinoma) and by following expression of stable non-hydroxylatable HIF-1α. Strikingly, ALS2 upregulation in hypoxia was required for Rab5 activation, tumor cell migration and invasion, as well as experimental metastasis in C57BL/6 mice. Finally, immunohistochemical analyses in patient biopsies with renal cell carcinoma showed that elevated HIF-1α correlates with increased ALS2 expression. Hence, this study identifies ALS2 as a novel hypoxia-inducible gene associated with tumor progression and metastasis.

scholarly journals Lipid metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3147
Author(s):  
Laurence Pellerin ◽  
Lorry Carrié ◽  
Carine Dufau ◽  
Laurence Nieto ◽  
Bruno Ségui ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Tumor Cell ◽  
Fatty Acid Synthase ◽  
Lipid Synthesis ◽  
Metabolic Reprogramming ◽  
Acid Uptake ◽  
Oncogenic Signaling ◽  
Tumor Cell Migration ◽  
Melanoma Progression

Metabolic reprogramming contributes to the pathogenesis and heterogeneity of melanoma. It is driven both by oncogenic events and the constraints imposed by a nutrient- and oxygen-scarce microenvironment. Among the most prominent metabolic reprogramming features is an increased rate of lipid synthesis. Lipids serve as a source of energy and form the structural foundation of all membranes, but have also emerged as mediators that not only impact classical oncogenic signaling pathways, but also contribute to melanoma progression. Various alterations in fatty acid metabolism have been reported and can contribute to melanoma cell aggressiveness. Elevated expression of the key lipogenic fatty acid synthase is associated with tumor cell invasion and poor prognosis. Fatty acid uptake from the surrounding microenvironment, fatty acid β-oxidation and storage also appear to play an essential role in tumor cell migration. The aim of this review is (i) to focus on the major alterations affecting lipid storage organelles and lipid metabolism. A particular attention has been paid to glycerophospholipids, sphingolipids, sterols and eicosanoids, (ii) to discuss how these metabolic dysregulations contribute to the phenotype plasticity of melanoma cells and/or melanoma aggressiveness, and (iii) to highlight therapeutic approaches targeting lipid metabolism that could be applicable for melanoma treatment.

scholarly journals Prodigiosin Inhibits Proliferation, Migration, and Invasion of Nasopharyngeal Cancer Cells

2018 ◽  
Vol 48 (4) ◽  
pp. 1556-1562 ◽  
Author(s):  
Yongze Liu ◽  
Han Zhou ◽  
Xiaofeng Ma ◽  
Chuanyao Lin ◽  
Ling Lu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Nasopharyngeal Cancer ◽  
Migration And Invasion ◽  
Boyden Chamber ◽  
Cell Cycle Distribution ◽  
Tumor Cell Migration

Background/Aims: Nasopharyngeal carcinoma remains a devastating and difficult disease to treat. This study explores the antineoplastic effect of prodigiosin on nasopharyngeal cancer cells. Methods: Human nasopharyngeal carcinoma CNE2 cells and human normal nasopharyngeal epithelial NP69 cells were obtained and treated with prodigiosin or fluorouracil (5-FU). Colony formation assay was performed to screen for the optimal experimental concentrations of prodigiosin and 5-FU, and MTT assay was used to examine cell proliferative ability. Flow cytometry was used to examine cell cycle distribution, the scratch test was employed to examine cell migration, and Transwell migration assay (Boyden chamber) was used to study cell invasion. Results: The optimal concentrations of prodigiosin and 5-FU for treatment were 4 mg/L and 0.35 mg/L, respectively. Both prodigiosin and 5-FU inhibited tumor cell proliferation. The percentage of cells in G0/G1 phase was higher and the percentage of cells in S phase was lower in the prodigiosin and 5-FU groups than in the untreated groups. Both prodigiosin and 5-FU inhibited tumor cell migration and tumor cell invasion. Conclusions: Our results suggest that prodigiosin can inhibit proliferation, migration, and invasion of nasopharyngeal carcinoma cells.

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